Structure and function Thyroid peroxidase (TPO) is a membrane-bound heme protein with a molecular weight of approximately 100,000. In the biosynthesis of thyroid hormones TPO is involved in 2 different reactions.
(1) Iodination of tyrosine residues.
(2) Oxidative coupling of 2 iodotyrosine residues on thyroid bead protein.
TPO requires both iodine and H2O2 to activate hormone synthesis. TPO function is described in the reference book, and TPO can be obtained from purification of the thyroid microsomal fraction, including trypsin digestion and clearance processing. Previously, thyroid microsomal fractions were often used as antigens to detect TPO antibodies; however, microsomal antibodies are also available in older literature.
TPOAb generally belongs to IgGI or IgG4 and varies with the case. TPOAb represents autoimmune thyroid disease or a risk of thyroid dysfunction.
I. Detection methods.
(1) Immunofluorescence test: This test is applied to frozen sections of the primate thyroid gland. Microsomal antibodies fluoresce on the top cytoplasm of thyroid epithelial cells, and the results are expressed in terms of potency.
(2) Passive hemagglutination reaction: Tannified red blood cells prepared for human thyroid microsomal treatment can passively coalesce into brown results, which are also expressed in potency.
(3) Immunoassay: This method uses encapsulated monoclonal antibodies TPOAb and TPOAb in serum with the addition of TPO labeled with radioisotopes or luminescence, followed by the precipitation of TPOAb with labeled TP complexes using protein A. or solid phase protein A in the form of Staphylococcus aureus, allowing the reaction mixture to be separated. Separation standards follow Medical Research Council (MRC) reference preparation 66/387, and this result is in kIU/L.
II. Indications.
(1) Elevated TSH of unknown etiology;
(2) Goiter of unknown etiology;
(3) Evaluation of suspected polyglandular autoimmune disease;
(4) Familial evaluation of autoimmune thyroid disease;
(5) Evaluation of the risk of developing thyroid disorders during treatment with thyroid drugs (e.g., lithium salts, amiodarone) or drugs acting on the immune system (e.g., cytokines, interferons);
(6) Risk screening for postpartum thyroiditis (during pregnancy or postpartum);
(7) Differential diagnosis of hyperthyroidism of unknown etiology.
Clinical Applications As with other thyroid antibodies, TPOAb may be positive in healthy individuals with perfectly normal thyroid function, especially in the elderly. For example, in a representative population after 85 years of age, 16% of women and 9% of men with no previous known thyroid dysfunction had TPOAb concentrations >100ku/L above the limit of detection.
Mild increases in TPOAb have been found in non-immune thyroid dysfunction, such as diseases in which the thyroid is in an autoimmune state or goiter, and likewise in some other autoimmune diseases, such as Addison’s disease, pernicious anemia, type 1 diabetes, leukoplakia, or diseases that activate the immune system, such as chronic active hepatitis, primary cholecystic fibrosis, or hepatitis C.
High levels of TPOAb (>2000ku/L) are almost always found in patients with HLADDR3 or DR5, and these haplotypes are associated with immune thyroid disease. In patients with Hashimoto’s thyroiditis, atrophic thyroiditis and postpartum thyroiditis, the rate of TPO elevation is 90%. In GD, the rate is slightly lower.
In autoimmune thyroid disease, TPO concentrations are consistent with clinical signs because TPOAb is used to destroy thyroid cells by activating complement and lymphocyte-mediated cell lysis.
TPOAb production in women can be inherited in an autosomal dominant manner.